The Ribosome and the Central Dogma of Molecular Biology

The Nobel Prize website usually does an excellent job of explaining the science behind the prizes. The STRUCTURE AND FUNCTION OF THE RIBOSOME is a good explanation of reasons why the 2009 Nobel Prize in Chemistry was awarded for work on the ribosome.

Unfortunately, the article begins by perpetuating a basic misunderstanding of the Central Dogma of Molecular Biology.

The ribosome and the central dogma. The genetic information in living systems is stored in the genome sequences of their DNA (deoxyribonucleic acid). A large part of these sequences encode proteins which carry out most of the functional tasks in all extant organisms. The DNA information is made available by transcription of the genes to mRNAs (messenger ribonucleic acids) that subsequently are translated into the various amino acid sequences of all the proteins of an organism. This is the central dogma (Crick, 1970) of molecular biology in its simplest form (Figure 1)

This is not the Central Dogma according to Crick (1970). I explain this in a posting from two years ago [Basic Concepts: The Central Dogma of Molecular Biology].

In both his original paper (Crick, 1958) and the 1970 update, Crick made it very clear that the Central Dogma of Molecular Biology is ....

The Central Dogma. This states that once “information” has passed into protein it cannot get out again. In more detail, the transfer of information from nucleic acid to nucleic acid, or from nucleic acid to protein may be possible, but transfer from protein to protein, or from protein to nucleic acid is impossible. Information means here the precise determination of sequence, either of bases in the nucleic acid or of amino acid residues in the protein.

The diagram that's usually attributed to the central dogma is actually the Sequence Hypothesis. Crick was well aware of the confusion and that's why he wrote the 1970 paper. It was at a time when the so-called "Central Dogma" had been "overthrown" byt the discovery of reverse transcriptase.

Since then the false version of the Central Dogma has been disproven dozens and dozens of times—it's a minor cottage industry.

Here's what Crick says about this false version of the Central Dogma in his 1970 paper—the one quoted at the top of this page.

It is not the same, as is commonly assumed, as the sequence hypothesis, which was clearly distinguished from it in the same article (Crick, 1958). In particular, the sequence hypothesis was a positive statement, saying that the (overall) transfer nucleic acid → protein did exist, whereas the central dogma was a negative statement saying that transfers from protein did not exist.

Let's try and get it right. It will have the great benefit of stopping us from putting up with any new papers that refute the Central Dogma of Molecular Biology!

It will also encourage critical thinking. Haven't you ever wondered why there is a Central Dogma when reverse transcriptase, splicing, epigenetics, post-translational modification, chromatin rearrangements, small regulatory RNAs, and just about everything else under the sun, supposedly refutes it?

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Crick, F.H.C. (1958) On protein synthesis. Symp. Soc. Exp. Biol. XII:138-163,

Crick, F. (1970) Central Dogma of Molecular Biology. Nature 227, 561-563. [PDF file]

2009 Nobel Prize in Chemistry

 
"for studies of the structure and function of the ribosome"

This one's not unexpected. Almost everyone knows that there should be a Nobel Prize for the ribosome [see Nobel Prize Predictions]. Problem is, Harry Noller was on most people's short list. He's been working on the problem since 1968 and has published more than 200 papers on ribosome structure and function. This is going to be a controversial decision.

Here's the press release.

Press Release

7 October 2009

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry for 2009 jointly to

Venkatraman Ramakrishnan, MRC Laboratory of Molecular Biology, Cambridge,
United Kingdom

Thomas A. Steitz, Yale University, New Haven, CT, USA

Ada E. Yonath, Weizmann Institute of Science, Rehovot, Israel


"for studies of the structure and function of the ribosome"


The ribosome translates the DNA code into life

The Nobel Prize in Chemistry for 2009 awards studies of one of life's core processes: the ribosome's translation of DNA information into life. Ribosomes produce proteins, which in turn control the chemistry in all living organisms. As ribosomes are crucial to life, they are also a major target for new antibiotics.

This year's Nobel Prize in Chemistry awards Venkatraman Ramakrishnan, Thomas A. Steitz and Ada E. Yonath for having showed what the ribosome looks like and how it functions at the atomic level. All three have used a method called X-ray crystallography to map the position for each and every one of the hundreds of thousands of atoms that make up the ribosome.

Inside every cell in all organisms, there are DNA molecules. They contain the blueprints for how a human being, a plant or a bacterium, looks and functions. But the DNA molecule is passive. If there was nothing else, there would be no life.

The blueprints become transformed into living matter through the work of ribosomes. Based upon the information in DNA, ribosomes make proteins: oxygen-transporting haemoglobin, antibodies of the immune system, hormones such as insulin, the collagen of the skin, or enzymes that break down sugar. There are tens of thousands of proteins in the body and they all have different forms and functions. They build and control life at the chemical level.

An understanding of the ribosome's innermost workings is important for a scientific understanding of life. This knowledge can be put to a practical and immediate use; many of today's antibiotics cure various diseases by blocking the function of bacterial ribosomes. Without functional ribosomes, bacteria cannot survive. This is why ribosomes are such an important target for new antibiotics.

This year's three Laureates have all generated 3D models that show how different antibiotics bind to the ribosome. These models are now used by scientists in order to develop new antibiotics, directly assisting the saving of lives and decreasing humanity's suffering.

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Another View of Science

I received this email message from Arv Edgeworth. It represents a serious point of view held by a large number of people. He gave me permission to post it. I'll respond in the comments.

I'm not a scientist, nor a professor of science, nor a son of a scientist, but I do love science.  I have collected over 150 science textbooks, that run from 1934 to 2006.  I'm responding to your article: "Do Graduate Students Understand Evolution?"  My greatest concern isn't that students views of evolution are flawed.  My greatest concern is not just with the students, but with professors as well, not understanding the limits of science.  I'm concerned that most professors at universities could not tell you where their science ends, and their philosophical worldview begins.  I believe modern science has a blindspot.  Sad to say, real science isn't what it used to be.

As the old science joke says: "Tell me who is funding the research, and I'll tell you the result."  I believe there are certain assumptions that the majority of scientists start out with today, based on their philosophical worldview, not the scientific evidence.  They interpret all the evidence in light of their worldview, then use their interpretation of the evidence as proof that their worldview is correct. Starting with different assumptions will always result in different conclusions.  My concern is that the majority of students, scientists, and professors of science cannot separate what they know from what they just believe, and I doubt if they would recognize the difference.

The amount of speculation and opinion that is being passed off as fact today in the name of science boggles the mind.  Scientific inquiry is being stiffled as students are not truly being trained how to think, they are just being told what to think.  Students many times are being indoctrinated, not educated.

I'm sure you are enamored with evolution theory, but why are trillions of dollars in funding and research being spent on trying to prove this theory is true, and we still don't have a cure for cancer?  Or do we?  I guess that could be debated.  After all, there is a lot of money in it.  How many scientists just spent 17 years trying to put Ardi's bones together from fossilized pieces of bone that were squished to smithereens and so badly decayed that a single touch turned the bones to dust?  One group of scientists gave conclusions of ape characteristics and one group gave conclusions of human characteristics.  Must be a "missing link."  I'm sure you probably dislike that term.  Could each group have had presuppositions?  I'm sorry but I have a hard time justifying this nonsense, and for what?  I had a dog that spent its whole life digging in the ground for bones too, but I never thought the government should pay his salary.

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Monday's Molecule #139

 
The molecule is 4-sulfonamide-2',4'-diaminobenzol or "Prontosil," a potent antibiotic. Gerhard Domagk received the Nobel Prize for developing Prontosil as a treatment against bacterial infections.

The overall winner is Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany. The undergraduate winner is Jason Oakley a biochemistry student at the University of Toronto.

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Name this molecule. The common name will do. Briefly describe what it does.

There's a Nobel Prize directly connected to this molecule. If you can name the molecule then you can find the Nobel Laureate(s).

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only four ineligible candidates for this week's reward: Philip Johnson of the University of Toronto, Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri and Joshua Johnson of Victoria University in Australia.

Frank and Joshua have agreed to donate their free lunch to an undergraduate. Consequently, I have an extra free lunch for a deserving undergraduate so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

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IDiots and Telomeres

 
Today's Nobel Prize announcement has prompted the usual stupidity from the creationist crowd. They don't get things right very often but when they rush into print their track record is even worse. You'd think they would have learned by now.

Most, but not all, bacteria have circular chromosomes. This is undoubtedly the primitive condition of living cells—at least once life got underway.

The advantage of a circular chromosome is that it doesn't have any free ends. This is important for two reasons: (1) nucleases that chew up nucleic acids like to work on free ends so having a circular chromosome increases the stability of the chromosome, and (2) circular chromosomes avoid the problems with replicating the ends of DNA.

That last reason needs a little explanation. DNA replication is complicated because evolution has only produced one kind of polymerase enzyme—the kind that works exclusively in the 5′→3′ direction.¹ This creates a problem when replicating double-stranded DNA because the strands run in opposite directions.

The DNA replication complex (replisome) has evolved a solution to this problem as illustrated in the diagram. As replication proceeds from right to left, one of the strands is copied directly by a DNA polymerase molecule. This new strand is called the leading strand. The other strand is copied by a separate DNA polymerase molecule but it has to run backwards. That strand, the lagging strand, is made in short pieces that have to be stitched together. Every now and then a new lagging strand fragment (Okazaki fragment) is initiated using a special RNA primer.

This is not a very good design but it's the only thing that could evolve given that polymerases can only go in one direction. Most of us could have easily designed an better way of replicating DNA if we were in charge. While we were at it we could have designed nucleases that don't attack genes.

The DNA replication complex may be messy but it works. At least it works with circular DNA. When you have free ends there's a bit of a problem. Look at the diagram. You can see that when the replication fork reaches the end on the left, the leading strand will be complete. However, there will likely be a gap at the very end where the lagging strand didn't initiate a new Okazaki fragment. When the replisome dissociates this gap will persist.

As strands continue to be replicated over and over there will be a progressive shortening of the chromosome because of the inefficiency of the replication process.

There are several ways of handling this problem. Some bacteriophage with linear chromosomes form circles during replication in order to avoid shortening. In bacteria, there are two different mechanisms for dealing with the problem. Either the ends of the two strand are covalently joined, creating a hairpin, or a protein is covalently attached to the end of one strand [see Bacterial Chromosomes]. Either way is effective in preventing chromosome shortening during replication.

Eukaryotes have evolved a third mechanism. The ends of eukaryotic chromosomes have extensive repeat segments called telomeres. This works because the repeats can be shortened for many generations before the "business part" of the chromosome is affected. The repeats can also be extended from time to time by telomerase. This restores the parts that are lost during replication. The copying is crude, but effective. It uses an RNA template that's part of the telomerase.

The net effect is that telomeres protect the ends of eukaryotic chromosomes. This protection is due to the fact that cells have nucleases that can chew up DNA and because the DNA replication machinery has a built-in flaw that doesn't allow it to copy the very ends of double-stranded DNA. All in all you'd have to say that if this was designed then it must have been Rube Goldberg who built it!

This year's Nobel Prize in Physiology & Medicine was awarded to Elizabeth Blackburn, Carol Greider and Jack Szostak for their work on telomeres and telomerase.

Within hours, DLH posted an article n Uncommon Descent [DNA Preservation discovery wins Nobel prize].

Were one to design the encoded DNA “blueprint” of life, would not one incorporate ways to preserve that “blueprint”? The Nobel prize in medicine has just been awarded for discovery of features that look amazingly like design to preserve chromosomes ....

These telomeres can probably be shown to be essential to survival, and are likely to be irreducibly complex. If so, how can macro evolution explain the origin of this marvelous preservation feature that appears to be an Intelligent Design?

Chromosome ends need "protection" because the designer couldn't figure out how to have safe nucleases in a cell and couldn't figure out how to replicate the ends of double-stranded DNA molecules. Several different mechanisms have evolved for dealing with these problems. Telomeres are one solution.

The telomeric repeats evolved from internal repeat sequences. Telomerase is a reverse transcriptase and it likely evolved from a retrovirus-encoded reverse transcriptase. In Drosophila there are no telomers and there isn't a telomerase, Instead, the chromosome ends are protected by multiple copies of defective transposons.

The IDiots are going to have to look elsewhere for evidence of God.

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1. There are good reasons for this. They have to do with the acccuracy of DNA replication and proofreading, but that's a story for another posting.

Mondays' Molecule #139

 
Name this molecule. The common name will do. Briefly describe what it does.

There's a Nobel Prize directly connected to this molecule. If you can name the molecule then you can find the Nobel Laureate(s).

The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only four ineligible candidates for this week's reward: Philip Johnson of the University of Toronto, Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri and Joshua Johnson of Victoria University in Australia.

Frank and Joshua have agreed to donate their free lunch to an undergraduate. Consequently, I have an extra free lunch for a deserving undergraduate so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

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Who's Smarter, Cats or Dogs?

 
Watch the Beagle escape.

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[Hat Tip: Greg Laden]

He Gets by with a Little Help from His Friends

 
I'm not a big fan of Canadian Prime Minister Stephen Harper but you gotta admire someone who sings a Beatles song with Yo-Yo Ma.

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2009 Nobel Prize in Physiology or Medicine

 
The 2009 Nobel Prize in Physiology or Medicine goes to Elizabeth Blackburn, Carol Greider, and Jack Szostak "for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase."

These scientists were on everyone's short list so there's no great surprise here.

Read all about it on the Nobel Prize website. Here's the press release.

Press Release

5 October 2009

The Nobel Assembly at Karolinska Institutet has today decided to award
The Nobel Prize in Physiology or Medicine 2009 jointly to

Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak

for the discovery of

"how chromosomes are protected by telomeres and the enzyme telomerase"

Summary

This year's Nobel Prize in Physiology or Medicine is awarded to three scientists who have solved a major problem in biology: how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.

The long, thread-like DNA molecules that carry our genes are packed into chromosomes, the telomeres being the caps on their ends. Elizabeth Blackburn and Jack Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation. Carol Greider and Elizabeth Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase.

If the telomeres are shortened, cells age. Conversely, if telomerase activity is high, telomere length is maintained, and cellular senescence is delayed. This is the case in cancer cells, which can be considered to have eternal life. Certain inherited diseases, in contrast, are characterized by a defective telomerase, resulting in damaged cells. The award of the Nobel Prize recognizes the discovery of a fundamental mechanism in the cell, a discovery that has stimulated the development of new therapeutic strategies.

The mysterious telomere

The chromosomes contain our genome in their DNA molecules. As early as the 1930s, Hermann Muller (Nobel Prize 1946) and Barbara McClintock (Nobel Prize 1983) had observed that the structures at the ends of the chromosomes, the so-called telomeres, seemed to prevent the chromosomes from attaching to each other. They suspected that the telomeres could have a protective role, but how they operate remained an enigma.

When scientists began to understand how genes are copied, in the 1950s, another problem presented itself. When a cell is about to divide, the DNA molecules, which contain the four bases that form the genetic code, are copied, base by base, by DNA polymerase enzymes. However, for one of the two DNA strands, a problem exists in that the very end of the strand cannot be copied. Therefore, the chromosomes should be shortened every time a cell divides – but in fact that is not usually the case

Both these problems were solved when this year's Nobel Laureates discovered how the telomere functions and found the enzyme that copies it.
Telomere DNA protects the chromosomes

In the early phase of her research career, Elizabeth Blackburn mapped DNA sequences. When studying the chromosomes of Tetrahymena, a unicellular ciliate organism, she identified a DNA sequence that was repeated several times at the ends of the chromosomes. The function of this sequence, CCCCAA, was unclear. At the same time, Jack Szostak had made the observation that a linear DNA molecule, a type of minichromosome, is rapidly degraded when introduced into yeast cells.

Blackburn presented her results at a conference in 1980. They caught Jack Szostak's interest and he and Blackburn decided to perform an experiment that would cross the boundaries between very distant species (Fig 2). From the DNA of Tetrahymena, Blackburn isolated the CCCCAA sequence. Szostak coupled it to the minichromosomes and put them back into yeast cells. The results, which were published in 1982, were striking – the telomere DNA sequence protected the minichromosomes from degradation. As telomere DNA from one organism, Tetrahymena, protected chromosomes in an entirely different one, yeast, this demonstrated the existence of a previously unrecognized fundamental mechanism. Later on, it became evident that telomere DNA with its characteristic sequence is present in most plants and animals, from amoeba to man.

An enzyme that builds telomeres

Carol Greider, then a graduate student, and her supervisor Blackburn started to investigate if the formation of telomere DNA could be due to an unknown enzyme. On Christmas Day, 1984, Greider discovered signs of enzymatic activity in a cell extract. Greider and Blackburn named the enzyme telomerase, purified it, and showed that it consists of RNA as well as protein (Fig 3). The RNA component turned out to contain the CCCCAA sequence. It serves as the template when the telomere is built, while the protein component is required for the construction work, i.e. the enzymatic activity. Telomerase extends telomere DNA, providing a platform that enables DNA polymerases to copy the entire length of the chromosome without missing the very end portion.

Telomeres delay ageing of the cell

Scientists now began to investigate what roles the telomere might play in the cell. Szostak's group identified yeast cells with mutations that led to a gradual shortening of the telomeres. Such cells grew poorly and eventually stopped dividing. Blackburn and her co-workers made mutations in the RNA of the telomerase and observed similar effects in Tetrahymena. In both cases, this led to premature cellular ageing – senescence. In contrast, functional telomeres instead prevent chromosomal damage and delay cellular senescence. Later on, Greider's group showed that the senescence of human cells is also delayed by telomerase. Research in this area has been intense and it is now known that the DNA sequence in the telomere attracts proteins that form a protective cap around the fragile ends of the DNA strands.

An important piece in the puzzle – human ageing, cancer, and stem cells

These discoveries had a major impact within the scientific community. Many scientists speculated that telomere shortening could be the reason for ageing, not only in the individual cells but also in the organism as a whole. But the ageing process has turned out to be complex and it is now thought to depend on several different factors, the telomere being one of them. Research in this area remains intense.

Most normal cells do not divide frequently, therefore their chromosomes are not at risk of shortening and they do not require high telomerase activity. In contrast, cancer cells have the ability to divide infinitely and yet preserve their telomeres. How do they escape cellular senescence? One explanation became apparent with the finding that cancer cells often have increased telomerase activity. It was therefore proposed that cancer might be treated by eradicating telomerase. Several studies are underway in this area, including clinical trials evaluating vaccines directed against cells with elevated telomerase activity.

Some inherited diseases are now known to be caused by telomerase defects, including certain forms of congenital aplastic anemia, in which insufficient cell divisions in the stem cells of the bone marrow lead to severe anemia. Certain inherited diseases of the skin and the lungs are also caused by telomerase defects.

In conclusion, the discoveries by Blackburn, Greider and Szostak have added a new dimension to our understanding of the cell, shed light on disease mechanisms, and stimulated the development of potential new therapies.

Elizabeth H. Blackburn has US and Australian citizenship. She was born in 1948 in Hobart, Tasmania, Australia. After undergraduate studies at the University of Melbourne, she received her PhD in 1975 from the University of Cambridge, England, and was a postdoctoral researcher at Yale University, New Haven, USA. She was on the faculty at the University of California, Berkeley, and since 1990 has been professor of biology and physiology at the University of California, San Francisco.

Carol W. Greider is a US citizen and was born in 1961 in San Diego, California, USA. She studied at the University of California in Santa Barbara and in Berkeley, where she obtained her PhD in 1987 with Blackburn as her supervisor. After postdoctoral research at Cold Spring Harbor Laboratory, she was appointed professor in the department of molecular biology and genetics at Johns Hopkins University School of Medicine in Baltimore in 1997.

Jack W. Szostak is a US citizen. He was born in 1952 in London, UK and grew up in Canada. He studied at McGill University in Montreal and at Cornell University in Ithaca, New York, where he received his PhD in 1977. He has been at Harvard Medical School since 1979 and is currently professor of genetics at Massachusetts General Hospital in Boston. He is also affiliated with the Howard Hughes Medical Institute.

References:

Szostak JW, Blackburn EH. Cloning yeast telomeres on linear plasmid vectors. Cell 1982; 29:245-255.
Greider CW, Blackburn EH. Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell 1985; 43:405-13.
Greider CW, Blackburn EH. A telomeric sequence in the RNA of Tetrahymena telomerase required for telomere repeat synthesis. Nature 1989; 337:331-7.

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Richard Dawkins on Tapestry

 
Here's a link to an interview of Richard Dawkins.

The world's most famous atheist sat down with Tapestry - a programme about religion - for an hour-long conversation. His chat with Mary Hynes encompassed evolution, Darwin, creationists, wildflowers, atheism and Dawkins' lingering affection for the Church of England(?!). Richard Dawkins is the author of The Greatest Show on Earth: The Evidence for Evolution, published by Free Press.

This is a really good interview. Mary Hynes did her homework and she asked some really good questions.

Listen, at the 20 minute mark, to Dawkins talk about Francis Collins and how he reconciles science and religion.

At 40 minutes Mary Hynes asks about the Newsweek interview and accommodationism. In case you don't want to listen to the podcast, I can assure you that Dawkins is not an accommodationist. She follows up with a discussion of "respect" and how religion should be treated.

Click on "Podcast" to hear the whole thing.

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Richard Dawkins on Bill Maher's Show

 
Here's Richard Dawkins appearing on Real Time with Bill Maher. Dawkins does a fine job of discussing evolution—it's very entertaining.

Equally entertaining is the second part where Maher gets politely raked over the coals for his silly views about Islamic terrorism. Now that I've been alerted to Maher's kooky ideas about medicine I'm seeing more and more examples of his strange way of thinking.

Richard Dawkins on Real Time with Bill Maher (10-2-09)
by Xrunner17

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[Hat Tip: RichardDawkins.net]

Ardi and Ida

 
"Ardi" is the nickname of Ardipithecus ramidus, the recently described hominid fossil. "Ida" is the nickname of Darwinius masillae, an early primate fossil that made a big splash last year.

The "Darwinius" affair has become notorious as a bad example of scientists getting into bed with book publishers, movie producers, and PR professionals [see The dangerous link between science and hype].

The "Ardi" publicity campaign seemed to be different. Sure, there's the 11 papers published simultaneously in Science—this clearly involves a coordinated attempt to maximize the impact of this fossil—but this seems like only a minor trangression. Coordinating publication happens lots of times.

But now there's the Discovery Channel documentary that's going to air next weekend.

A DISCOVERY CHANNEL EXCLUSIVE, WORLD PREMIERE SPECIAL BRINGS YOU THE STORY OF THE LATEST NEWS ABOUT HUMAN EVOLUTION

DISCOVERING ARDI airs Sunday, October 11 at 9 PM (ET/PT)

Following publication in the journal Science on the discovery and study of a 4.4 million-year-old female partial skeleton nicknamed "Ardi," Discovery Channel will present a world premiere special, DISCOVERING ARDI, Sunday October 11 at 9 PM (ET/PT) documenting the sustained, intensive investigation leading up to this landmark publication of the Ardipithecus ramidus fossils.

UNDERSTANDING ARDI, a one-hour special produced in collaboration with CBS News will air at 11 PM (ET/PT) immediately following DISCOVERING ARDI. The special is moderated by former CBS and CNN anchor Paula Zahn and includes research team members Dr. Tim White, Dr. Yohannes Haile-Selassie, Dr. Giday WoldeGabriel, Dr. Owen Lovejoy, and science journalist Ann Gibbons

The scientific investigation began in the Ethiopian desert 17 years ago, and now opens a new chapter on human evolution, revealing the first evolutionary steps our ancestors took after we diverged from a common ancestor we once shared with living chimpanzees. "Ardi's" centerpiece skeleton, the other hominids she lived with, and the rocks, soils, plants and animals that made up her world were analyzed in laboratories around the world, and the scientists have now published their findings in the prestigious journal Science.

"Ardi" is now the oldest skeleton from our (hominid) branch of the primate family tree. These Ethiopian discoveries reveal an early grade of human evolution in Africa that predated the famous Australopithecus nicknamed "Lucy." Ardipithecus was a woodland creature with a small brain, long arms, and short legs. The pelvis and feet show a primitive form of two-legged walking on the ground, but Ardipithecus was also a capable tree climber, with long fingers and big toes that allowed their feet to grasp like an ape's. The discoveries answer old questions about how hominids became bipedal.

The international research team weighed in on the scope of the project and its findings:

"These are the results of a scientific mission to our deep African past," said project co-director and geologist, Dr. Giday WoldeGabriel of the Los Alamos National Laboratory.

"The novel anatomy that we describe in these papers fundamentally alters our understanding of human origins and early evolution," said project anatomist and evolutionary biologist, Professor C. Owen Lovejoy, Kent State University.

Project co-director and paleontologist Professor Tim White of the Human Evolution Research Center at the University of California Berkeley adds, "Ardipithecus is not a chimp. It's not a human. It's what we used to be."

DISCOVERING ARDI begins its story with the 1974 discovery of Australopithecus afarensis in Hadar, northeastern Ethiopia. Nicknamed "Lucy," this 3.2 million year old skeleton was, at the time, the oldest hominid skeleton ever found. As the Discovery Channel special documents, Lucy's title would be overtaken twenty years later by the 1994 discovery of "Ardi" in Ethiopia's Afar region in the Middle Awash study area. It would take an elite international team of experts the next fifteen years to delicately, meticulously and methodically piece together "Ardi" and her lost world in order to reveal her significance.

We all know that this documentary took a long time to make. That means the authors of the scientific papers were cooperating with Discovery Channel (and CBS News?) long before the papers were published. Perhaps even before the papers were accepted.

Something isn't right about all of this. John Hawks senses it too ["Discovering Ardi"].

Oh, my. Well it stands to reason that something this coordinated wasn't just science. I wonder whether anyone will ask the questions about the timing of Science's publication and the documentary release only a week later.

I have to tell you, I've been wondering about all the bogus-looking Darwin paraphrases these guys have been throwing out -- you know, the ones about how Darwin taught us about how chimpanzees changed from their common ancestors, and how fossil humans would tell us about the apes. I can't find anything like that in any of Darwin's publications -- please e-mail if it's there and I'm missing it.

But now I see where they're coming from. It's the tagline from the Discovery show!

I smell a rat.

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Do Graduate Students Understand Evolution?

 
The other day I was discussing how to teach evolution with one of my colleagues and the discussion turned to the presumed distinction between students who were really interested in science and everyone else. My colleague claimed that students who were science oriented probably managed to acquire a good understanding of evolution in spite of the fact that some undergraduate courses weren't doing a very good job of teaching the subject.

I pointed out that my impression was different. I suggested that most Professors in our department don't have a firm grasp of one of the most fundamental concepts in biology (evolution), and neither do our graduate students. I reminded my colleague of the times when we cringe at graduate student presentations when the topic of evolution comes up.

Ryan Gregory must have felt the same way since he was prompted to do a survey of graduate students in science departments at Guelph University. The result is published in BioScience. You can read about it on Ryan's blog: How well do grad students grasp evolution?.
Here's the press release...

Science Students Could Brush Up On Darwin, U of G Study Finds

October 01, 2009 - News Release

Even students pursuing advanced degrees in science could brush up on their knowledge of evolution, according to a new study by University of Guelph researchers.

The finding reveals that there is room for improvement in how evolution is taught from elementary school up, said Ryan Gregory, a professor in Guelph’s Department of Integrative Biology, who conducted the research with former student Cameron Ellis.

The study was published today in BioScience. It’s particularly timely, given that this year is the bicentennial of Charles Darwin’s birth and the 150th anniversary of publication of On the Origin of Species, which underpins understanding of the diversity of Earth’s organisms and their interrelations.

“Misconceptions about natural selection may still exist, even at the most advanced level,” Gregory said.

“We’re looking at a subset of people who have spent at least four years, sometimes even six or seven years, in science and still don’t necessarily have a full working understanding of basic evolutionary principles or scientific terms like ‘theories.’”

Many previous studies have assessed how evolution is understood and accepted by elementary, high school and undergraduate students, as well as by teachers and the general public, Gregory said. But this was the first to focus solely on students seeking graduate science degrees.

The study involved nearly 200 graduate students at a mid-sized Canadian university who were studying biological, physical, agricultural or animal sciences. About half of the students had never taken an evolutionary biology course, which is often not a prerequisite.

The researchers found that the vast majority of the students recognized the importance of evolution as a central part of biology. Overall, they also had a better understanding of evolutionary concepts than most people.

“That was encouraging, especially because it was across several colleges — it wasn’t just the biology students,” Gregory said.

But when the students were asked to apply basic evolutionary principles, only 20 to 30 per cent could do so correctly, and many didn’t even try to answer such questions. Of particular interest to Gregory is the finding that many students seem less than clear about the nature of scientific theories.

“This is telling us that traditional instruction methods, while leading to some basic understanding of evolution, are not producing a strong working knowledge that can be easily applied to real biological phenomena.”

Gregory has studied evolution-related topics for years and recently co-organized a workshop designed to improve how the subject is taught in public schools. He is also associate editor of Evolution: Education and Outreach, a journal written for science teachers, students and scientists. He recently created Evolver Zone, a free online resource for anyone interested in evolutionary biology.
He is also helping bring an evolution-inspired art exhibit to U of G this month. “This View of Life: Evolutionary Art in the Year of Darwin, 2009” highlights diverse artists’ views of Darwin’s ideas and evolution in general. It runs Oct. 9 to 30 in the science complex atrium.

Some of us know what the problem is. What are we going to do about it? How are we going to convince professors that evolution education has to change when most of them don't even recognize there's a problem because their own views of evolution are flawed?

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Denyse O'Leary Making Sense

 
Like they say, even a stopped clock is right twice a day. I'm happy to report that this is one of those days when Denyse O'Leary says something intelligent [Fun with Mark Steyn: But when isn’t Mark Steyn fun?].

Darwinists are forever nagging the keepers of the public purse to generously fund their efforts to sell their story to a disbelieving public, but the money is wasted by definition. The reason people don’t believe a lot of this stuff is that it isn’t believable. More public relations will actually make more people aware of scandals like “Ida” or the fact that there is little or no response to the ridiculous claims of “evolutionary psychology” – which make the science press sound like the National Enquirer.

It's a sad day, actually, when an Intelligent Design Creationist points out something that many scientists are ignoring.

Scientists are very good at self-promotion but that's not compatible with good science. We need more good science journalists.¹ That's the group that has to face up to to their failures in the past and start to clean up their acts.

They will soon be extinct if they don't.

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1. I do not mean to imply that Denyse O'Leary is an example of a good science journalist.

Map That Campus Returns

 
After a lengthy hiatus, the ever-popular feature on Alex Pallazzo's blog has returned. See Map That Campus XLVII. (Extra bonus points if you can translate XLVII into a real number!)

There's actually three campuses this week. You need to get all three before you can pat yourself on the back. No looking at the comments before giving your answer!

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